Schreurs A J, Verhoef J, Nijkamp F P
Eur J Pharmacol. 1983 Jan 28;87(1):127-32. doi: 10.1016/0014-2999(83)90058-4.
Infections of the deeper respiratory airways can contribute to the progression of chronic asthmatic bronchitis. In the present report a number of microorganisms affecting the number of beta-adrenoceptors in guinea-pig lung homogenates are described. Haemophilus influenzae, Streptococcus pneumoniae, Bordetella pertussis and Escherichia coli O111B4 induced a significant decrease of the number of beta-adrenoceptors (by approximately 20%). Staphylococcus aureus, influenza A virus and Escherichia coli J5 were not active. These data point to a common factor shared by gram-negative bacilli; i.e. endotoxin. Purified endotoxin of E. coli O111B4 also decreased the number of beta-adrenoceptors, while E. coli J5-LPS did not. This suggests that neutral polysaccharides of bacterial cell walls, especially those in the 'O'-antigenic side chain of gram-negative endotoxins may be responsible for the decrease of beta-adrenoceptor number and therefore contribute to the pathogenesis of chronic asthmatic bronchitis. Intact endotoxin seems to be necessary since neither the isolated lipid nor the polysaccharide part of E. coli O111B4 LPS affected the number of beta-adrenoceptors in the lung.
深部呼吸道感染可促使慢性哮喘性支气管炎病情进展。在本报告中，描述了一些影响豚鼠肺匀浆中β - 肾上腺素能受体数量的微生物。流感嗜血杆菌、肺炎链球菌、百日咳博德特氏菌和大肠杆菌O111B4可使β - 肾上腺素能受体数量显著减少（约20%）。金黄色葡萄球菌、甲型流感病毒和大肠杆菌J5则无此作用。这些数据表明革兰氏阴性杆菌存在一个共同因素，即内毒素。大肠杆菌O111B4的纯化内毒素也可减少β - 肾上腺素能受体数量，而大肠杆菌J5 - LPS则无此作用。这表明细菌细胞壁的中性多糖，尤其是革兰氏阴性内毒素“O”抗原侧链中的多糖，可能是导致β - 肾上腺素能受体数量减少的原因，因此在慢性哮喘性支气管炎的发病机制中起作用。完整的内毒素似乎是必需的，因为大肠杆菌O111B4 LPS的分离脂质部分和多糖部分均不影响肺中β - 肾上腺素能受体的数量。
